TOKYO - Japan on Friday rebuffed Washington's demands that Tokyo ease its terms for lifting a ban on U.S. beef imports, imposed two years ago because of fears of mad cow disease.

U.S. Agriculture Secretary Mike Johanns had earlier insisted that cows younger than 30 months are considered safe from mad cow disease, and can be imported. Japan wants to set the limit at 21 months.

"We have received no formal request (from Washington), and even if we did receive one, we're not in a position to say yes," Japan's Agriculture Minister Shoichi Nakagawa said Friday.

He said Japan would study the issue.

"Our focus is on ensuring safety and gaining public consent," he said.

Tokyo banned American beef in December 2003 after the discovery of the first U.S. case of mad cow disease.

Japan was then the most lucrative overseas market for U.S. beef, and an increasingly impatient Washington has pushed hard for the ban to be lifted.

Earlier this week, Japan's food safety commission approved a report saying the mad cow disease risk in U.S. beef was minuscule as long as imports were limited to meat from cows under 21 months, and all brain and spinal cord matter was removed.

Japan is expected to reach a decision on the matter by the end of the year, after monthlong public hearings that began this week.

Johanns has criticized the commission's report, saying the conditions are too stringent.

"The science is very, very clear that in animals under 30 months, you just don't have a (mad cow disease) problem," Johanns said Thursday. "So obviously we hope to continue to open up the marketplace."

Many scientists believe that beef from cattle infected with mad cow disease, or bovine spongiform encephalopathy, can cause a fatal brain disorder in humans.

Japanese consumers remain deeply wary of U.S. beef, with recent polls showing that nearly 70 percent opposed lifting the ban.

http://www.dfw.com/mld/dfw/news/breaking_news/13085547.htm

i don't believe johanns could tell the truth if the world depended on it.

>Under this proposal, ruminant and ruminant products eligible for entry into>the United States from a BSE minimal risk region would include:>>1) bovine>animals less than 30 months of age for immediate slaughter;>>2) bovine>animals for feeding to be moved to a designated feedlot and then to>slaughter at less than 30 months of age; >snip...

>6) fresh (chilled or frozen)>meat from bovines less than 30 months of age; 7) fresh (chilled or frozen)>whole or half carcasses of bovines less than 30 months of age; 8) fresh>(chilled or frozen) bovine liver; 9) fresh (chilled or frozen) bovine>tongues;

the myth that cattle under 30 months of age are free from BSE/TSE is just that, a myth,and it's a false myth !

The implications of the Swiss result for Britain, which has had the mostBSE, are complex. Only cattle aged 30 months or younger are eaten inBritain, on the assumption, based on feeding trials, that cattle of thatage, even if they were infected as calves, have not yet accumulatedenough prions to be infectious. But the youngest cow to develop BSE onrecord in Britain was 20 months old, showing some are fast incubators.Models predict that 200-300 cattle under 30 months per year are infectedwith BSE and enter the food chain currently in Britain. Of these 3-5could be fast incubators and carrying detectable quantities of prion.

Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s145d.pdf

2

6. It also appears to me that Mr Bradley's answer (that it would take lessthan say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprisethat it

could take as little of 1 gram of brain to cause BSE by the oral routewithin the

same species. This information did not become available until the "attackrate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used toensure

that the actual result was within both a lower and an upper limit within thestudy

and the designing scientists would not have expected all the dose levels totrigger

infection. The dose ranges chosen by the most informed scientists at thattime

ranged from 1 gram to three times one hundred grams. It is clear that thedesigning

scientists must have also shared Mr Bradley's surprise at the resultsbecause all the

dose levels right down to 1 gram triggered infection.

http://www.bseinquiry.gov.uk/files/ws/s147f.pdf

Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm

2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml

NEW MAD COW STRAIN CALLED BASE, VERY SIMILAR TO SPORADIC CJD IN HUMANS;

Edited by Stanley B. Prusiner, University of California, San Francisco, CA,and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, aremammalian neurodegenerative disorders characterized by a posttranslationalconversion and brain accumulation of an insoluble, protease-resistantisoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human andanimal TSE agents exist as different phenotypes that can be biochemicallydifferentiated on the basis of the molecular mass of the protease-resistantPrPSc fragments and the degree of glycosylation. Epidemiological, molecular,and transmission studies strongly suggest that the single strain of agentresponsible for bovine spongiform encephalopathy (BSE) has infected humans,causing variant Creutzfeldt-Jakob disease. The unprecedented biologicalproperties of the BSE agent, which circumvents the so-called "speciesbarrier" between cattle and humans and adapts to different mammalianspecies, has raised considerable concern for human health. To date, it isunknown whether more than one strain might be responsible for cattle TSE orwhether the BSE agent undergoes phenotypic variation after naturaltransmission. Here we provide evidence of a second cattle TSE. The disorderwas pathologically characterized by the presence of PrP-immunopositiveamyloid plaques, as opposed to the lack of amyloid deposition in typical BSEcases, and by a different pattern of regional distribution and topology ofbrain PrPSc accumulation. In addition, Western blot analysis showed a PrPSctype with predominance of the low molecular mass glycoform and aprotease-resistant fragment of lower molecular mass than BSE-PrPSc.Strikingly, the molecular signature of this previously undescribed bovinePrPSc was similar to that encountered in a distinct subtype of sporadicCreutzfeldt-Jakob disease.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheepand goats were transmitted to squirrel monkeys (Saimiri sciureus) that wereexposed to the infectious agents only by their nonforced consumption ofknown infectious tissues. The asymptomatic incubation period in the onemonkey exposed to the virus of kuru was 36 months; that in the two monkeysexposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months,respectively; and that in the two monkeys exposed to the virus of scrapiewas 25 and 32 months, respectively. Careful physical examination of thebuccal cavities of all of the monkeys failed to reveal signs or orallesions. One additional monkey similarly exposed to kuru has remainedasymptomatic during the 39 months that it has been under observation.